Regulatory mechanism of non-coding RNA in osteoarthritis and the research on traditional Chinese medicine intervention
- VernacularTitle:非编码RNA对骨关节炎的调控机制及中药干预研究进展
- Author:
Fanzhuo HUANG
1
;
Yuan LI
2
;
Xuan ZHANG
1
;
Yuan LIU
1
Author Information
1. College of Orthopedics and Traumatology，Guangxi University of Chinese Medicine，Nanning 530001，China
2. Nursing Department，Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine，Nanning 530011，China
- Publication Type:Journal Article
- Keywords:
osteoarthritis;
traditional Chinese medicine;
compound formula;
non-coding RNA;
regulatory mechanism
- From:
China Pharmacy
2025;36(14):1819-1824
- CountryChina
- Language:Chinese
-
Abstract:
Osteoarthritis （OA） is a chronic degenerative disease characterized primarily by the degeneration of articular cartilage， with its pathogenesis involving a multifactorial interplay of inflammatory responses， chondrocyte apoptosis， and extracellular matrix （ECM） degradation. Non-coding RNA （ncRNA） participates in the occurrence and development of OA through their diverse regulatory pathways， providing new potential targets for its treatment. This paper systematically elucidates the mechanisms of ncRNA [micro ncRNA （miR）， circular ncRNA （circR）， and long ncRNA （lncR）] in regulating OA ， as well as the current research status of traditional Chinese medicine （TCM） intervening in OA by modulating ncRNA. It is found that ncRNA participate in the pathological processes of OA by constructing a multi-layered regulatory network： miR inhibits the translation of key target genes and regulate downstream signaling pathways； circR can act as ‘molecular sponges’ to competitively absorb miRs for indirect regulation， as well as directly modulate protein functions； lncR possess both ‘molecular sponge’ capabilities and the ability to intervene directly in pathways. Andrographolide， Xinfeng capsules and others intervene in the OA process by regulating the expression of miR， forming a ‘TCM-miR-downstream response chain’， which reduces the expression of matrix-hydrolyzing enzymes and inhibits the secretion of inflammatory factors； paeoniflorin， Rongjin niantong formula and others intervene in the OA process by affecting circR and lncR， thereby forming a ‘TCM-lncR/circR-miR-downstream response chain’ to promote chondrocyte proliferation and reduce ECM degradation.
